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Objective: Using new lipidomic analyses employing high performanceliquid chromatography coupled with a tandem mass spectrometer, a novelseries of endogenous mediator resolvinD1was quantified in acute lunginjury rats lung tissues.Methods：One hundred and thirty eight male Sprague-Dawley rats wereincluded, and their lung’s tissues exploited to detect and quantify RvD1level after inducing acute lung injury (ALI) by lipopolysaccharide(2mg/kg, LPS). Rats were observed at6h,12h,1d,2d,3d,4d,5d,6d,7d,8d,9d and10d after LPS was administrated, then they were euthanasia.We collected bronchoalveolar lavage fluid (BALF) and the lung tissuesfor further analysis. Paraffin section and HE dyeing of the lung tissueswere for histopathology observations; IL-6and IL-10were detected byELISA; lungs were gently homogenized for lipidomic analysesemploying high performance liquid chromatography coupled with atandem mass spectrometer. Results：Compared with LPS and the blank group, the connection ofendogenous RvD1concentration and the level of lung tissueinflammation have obvious correlation. RvD1level variation trend andcytokines have the subtle connections in line with the fierceinflammation.Conclusions：RvD1will be autocrined by cell-cell interaction thoughtranscellular pathway during the acute inflammatory response. Our studyshowed that without foreign intervention, RvD1was produced at a basicconcentration. When inflammation arose, RvD1participated in theinflammatory response beginning and progressing.RvD1endogenousconcentration decreased until tissue healed, which concentration wasrestored to normal level.
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